About

Tom Lin is a professor leading the Tom Lin Lab of Medicinal Proteomics at Rutgers University. His research focuses on utilizing proteomics to discover post-translational modifications (PTMs) in the whole proteome, integrating medicinal chemistry to innovate drug discovery and development, and exploring cell biology to understand PTM functions in human diseases. His lab aims to improve the quality of life by curing diseases and advancing knowledge of cell functions through creative and rigorous research at the interface of proteomics and medicinal chemistry. Professor Lin emphasizes a fair, transparent, respectful, and supportive research environment, fostering next-generation scientists capable of learning, creating, and conducting independent projects. His lab not only hosts employees but also incubates future scientists and leaders, promoting collaboration and growth. His work contributes to the development of therapeutic strategies based on protein modification systems, with a broader goal of advancing medical science and drug discovery.

Research topics

• Biology
• Immunology
• Molecular biology
• Cancer research
• Pathology

Selected publications

• MOLECULAR MARKERS IN OSTEOSARCOMA – A cDNA MICROARRAY AND RT-PCR ANALYSIS

  Journal of Musculoskeletal Research · 2005-06-01

  article

  Osteosarcomas account for about 20% of all primary bone neoplasms, and affect predominantly adolescents. Important prognostic factors include the presence or absence of metastases at the time of presentation and tumor response to neoadjuvant chemotherapy. Biological markers predicting metastases and chemoresistance are not well characterized. cDNA microarray analysis enables one to examine the expression of thousands of genes in tumor samples. We performed cDNA microarray analysis of histologically low and high grade areas in osteosarcomas to identify gene expression patterns which may depict aggressive behavior. Microarray analysis with 1.2 K cancer array revealed many differentially expressed genes (both upregulated and downregulated), in histologically high grade tumor samples as compared with a low grade sample. Selected up and down regulated markers in the high grade sarcomas were tested in a group of high grade osteosarcomnas (OS) with varying responses to chemotherapy. Of the multiple markers analyzed, ezrin, a member of the ERM family of membrane-cytoskeleton linkers showed an expression pattern statistically significant between tumors with good response to chemotherapy compared with tumors with poor response (p = 0.036). We discuss our findings, with current review of literature.

  PublisherDOI

• GENE EXPRESSION ANALYSIS OF A DEDIFFERENTIATED LIPOSARCOMA — DIFFERENCES BETWEEN HIGH AND LOW GRADE AREAS: ANALYSIS OF TWO CASES AND LITERATURE REVIEW

  Journal of Musculoskeletal Research · 2005-03-01 · 2 citations

  article

  The phenomenon of dedifferentiation typically occurs in soft tissue sarcomas where a low grade or well-differentiated tumor shows an abrupt transformation to a high-grade sarcoma without lineage specificity. The biological behavior and metastatic potential of these tumors is dictated by the dedifferentiated phenotype. Tumor material was available from two dedifferentiated liposarcomas. We performed cDNA microarray analysis of a dedifferentiated liposarcoma in which the atypical lipomatous/well-differentiated and dedifferentiated portions were grossly distinct, to find differentially expressed genes in the dedifferentiated component compared to the well-differentiated component. There were 100 differentially expressed genes, both up- and down-regulated in the high grade sarcoma. In addition, we performed RT-PCR on selected genes in both cases to confirm the microarray findings. We discuss the expression patterns of these genes in comparison to other studies in the literature.

  PublisherDOI

• Flow Cytometric Quantitation of Lymphocyte Subsets among HIV-infected and-uninfected Infants in the First Year of Life † 872

  Pediatric Research · 1998-04-01

  articleOpen access1st authorCorresponding
  PublisherOA PDFDOI

• Altered CD45 Expression in Malignant B-1 Cells

  Cellular Immunology · 1996-05-01 · 14 citations

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• Regulatory aspects of clonally expanded B-1 (CD5+B) cells

  International Journal of Clinical & Laboratory Research · 1992-03-01 · 11 citations

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• IL-10 production in a CD5+ B cell lymphoma arising in a CD4 monoclonal antibody-treated SJL mouse

  Clinical Immunology and Immunopathology · 1992-10-01 · 20 citations

  article1st authorCorresponding
  PublisherDOI

• Syngeneic B Lymphoma Cells Provide a Unique Stimulus to Natural Killer (NK) Cells in Genetically Low-NK SJL/J Mice

  Journal of Leukocyte Biology · 1991-01-01 · 8 citations

  article1st authorCorresponding

  SJL/J mice are a genetically low-NK strain, and their cytotoxic activity cannot be augmented with conventional NK inducers. In contrast, effector cells taken from the lymphoid tissues of SJL mice bearing a syngeneic B cell lymphoma (RCS) show variable, but significant levels of cytotoxic activity against NK-susceptible targets, such as YAC-1. Previous results suggested that the RCS cells themselves contributed to this cytotoxicity. However, results presented here indicate the most, if not all of the activity present within the lymphoid tissues of RCS-bearing mice is mediated by RCS-activated, host NK cells. These results were confirmed by in vitro studies, which demonstrate that both gamma irradiated (gamma-) RCS cells and gamma-allogeneic spleen cells induce cytotoxic activity in SJL spleen cells against YAC targets. However, the cytotoxicity induced by gamma-allogeneic cells is mediated largely by lymphokine-activated killer (LAK) cells, since these effectors also lyse NK-resistant target cells, such as L1210. In contrast, the cytotoxic effector cells that are induced by syngeneic gamma-RCS cells cause lysis of YAC targets, but not L1210 target cells. These data indicate that the syngeneic B cell lymphomas of SJL mice are a unique stimulus for host NK cells in this strain. Since activated NK cells produce a variety of lymphokines, RCS stimulation of host NK cells in SJL mice may provide some of the growth-promoting lymphokines that are known to be necessary for progressive growth of these lymphoma cells.

  PublisherDOI

• Influence of Host Environment on Growth of Clonal CD5 ⁺ B (Lyl ⁺ B) Cells

  Autoimmunity · 1991-01-01 · 1 citations

  article

  Autoimmune NZB mice have increased percentages of CD5+B (Lyl+B) cells in both the spleen and peritoneum. We have previously reported that as NZB mice age they develop a clonal population of hyperdiploid CD5+B cells in the spleen. These cells can readily be transplanted into unirradiated recipients. The growth characteristics of such transplanted hyperdiploid NZB spleen cells were examined in different recipient strains to determine if the immunological status of the host environments affected the growth of the clonal CD5+B cells. Young NZB and NZB.xid recipients (lacking hyperdiploid CD5+B cells) allowed growth and expansion of unpassaged CD5+B cells derived from primary NZB mice. Similarly, (NZBxDBA/2) and (NZBxBALB/c) F1 recipients allowed for expansion of CD5+B cell clones from primary sources. In a separate experiment, T cell-depleted NZB spleen cells containing a hyperdiploid CD5+B cell clone were transferred to SCID mice. The SCID environment supported the growth of the primary clone. None of these recipients normally have elevated CD5+B cells, yet these recipients allowed growth of primary transferred hyperdiploid cells. However, a difference in the ability of these recipient strains in their ability to expand multiply passaged CD5+B cell clones was observed. These results indicate that while hyperdiploid CD5+B cells are difficult to be maintained in culture, they can readily be passaged in vivo. The host environment may provide growth factors or signals for endogenous growth factors. Although the CD5+B clones arise initially in a hyperactive autoimmune environment, a hyperimmune environment is not necessary to support their growth. Transferred CD5+B cells affect the recipient environment and reduce the percentages of normal B cells.

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Frequent coauthors

• Helen Fernandes

  Universidade Estadual da Região Tocantina do Maranhão

  16 shared

• Elizabeth Raveché

  12 shared

• Frederick D. Coffman

  Rutgers, The State University of New Jersey

  8 shared

• Nicholas M. Ponzio

  8 shared

• Marion C. Cohen

  8 shared

• Seena C. Aisner

  8 shared

• Stanley Cohen

  8 shared

• Meera Hameed

  8 shared

Awards & honors

• Rutgers Start-up Fund
• NCI R21 Award
• NHLBI R01 Award